∆nFGF1 Protects β-Cells against High Glucose-Induced Apoptosis via the AMPK/SIRT1/PGC-1α Axis

Figure 5

∆nFGF1 inhibits glucolipotoxicity-induced apoptosis in MIN6 cells via AMPK/SIRT1/PGC-1α signaling. MIN6 cells were exposed to NG (11.1 mM) and HG+PA (33 mM HG+0.5 mM PA) with or without the AMPK inhibitor Compound C (CC) in the presence or absence of ∆nFGF1 for 24 h. (a) The protein levels of p-AMPK, SIRT1, and PGC-1α analyzed by Western blot (left panel) and quantified by ImageJ (right panels) (). (b) The protein expression levels of Bcl-2, Bax, and C-caspase 3 analyzed by Western blot (left panel) and quantified by ImageJ (right panels) (). (c) MIN6 cells were transfected with AMPK siRNA for 48 h before exposure to NG (11.1 mM) and HG+PA (33 mM HG+0.5 mM PA) in the presence or absence of ∆nFGF1 for 24 h. The protein expression levels of p-AMPK, SIRT1, and PGC-1α analyzed by Western blot (left panel) and quantified by ImageJ (right panels) (). (d) The protein expression levels of Bcl-2, Bax, and C-caspase 3 analyzed by Western blot (left panel) and quantified by ImageJ (right panels) (). β-Actin was used as a loading control. (e) Apoptosis of β-cells in each group was evaluated by flow cytometry analysis. The apoptotic rate was calculated as the percentage of Annexin V-positive cells divided by the total number of cells. (f) Schematic diagram illustrating the model of ∆nFGF1-mediated inhibition of pancreatic β-cell apoptosis in T2DM. All data are presented as . , , and . n.s.: no significance.

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